中国临床营养杂志
中國臨床營養雜誌
중국림상영양잡지
CHINESE JOURNAL OF CLINICAL NUTRITION
2009年
2期
91-94,Ⅰ
,共5页
陈雪峰%何桂珍%董良广%崔晓雨%舒红%王秀荣%范东梅
陳雪峰%何桂珍%董良廣%崔曉雨%舒紅%王秀榮%範東梅
진설봉%하계진%동량엄%최효우%서홍%왕수영%범동매
肠道缺血再灌注损伤%高迁移率族蛋白%肠黏膜屏障%肠淋巴液引流
腸道缺血再灌註損傷%高遷移率族蛋白%腸黏膜屏障%腸淋巴液引流
장도결혈재관주손상%고천이솔족단백%장점막병장%장림파액인류
Intestine ischemia-reperfusion injury%High mobility group box 1%Gut barrier%Drainage of in- testine lymph fluid
目的 研究大鼠肠道缺血再灌注损伤时,内源性配体高迁移率族蛋白1(HMGB1)的变化及淋巴引流对肠屏障损伤的影响.方法 32只健康雄性SPF级SD大鼠随机分为空白组、假手术组、肠道缺血再灌注组(I/R)和肠道缺血再灌注+淋巴液引流组(I/R+引流组),每组8只.在缺血再灌注损伤后检测肠道损伤程度、HMGB1变化、内毒素移位情况及循环细胞因子.结果 I/R组和I/R+引流组大鼠的肠道损伤程度、内毒素水平、HMGB1和各炎症因子水平均显著高于空白组和假手术组(P<0.05);I/R组内毒素水平和各炎症因子显著高于I/R+引流组(P<0.05).免疫组织化学染色结果 显示,I/R组的HMGBI表达显著高于I/R+引流组.结论 缺血再灌注损伤可导致大鼠体内HMGB1水平升高和肠黏膜屏障损伤,HMGB1可能增加肠屏障损伤和系统炎症反应.肠淋巴引流能阻断肠.淋巴途径,改善肠屏障形态和功能,减少循环中炎症因子和内毒素水平.
目的 研究大鼠腸道缺血再灌註損傷時,內源性配體高遷移率族蛋白1(HMGB1)的變化及淋巴引流對腸屏障損傷的影響.方法 32隻健康雄性SPF級SD大鼠隨機分為空白組、假手術組、腸道缺血再灌註組(I/R)和腸道缺血再灌註+淋巴液引流組(I/R+引流組),每組8隻.在缺血再灌註損傷後檢測腸道損傷程度、HMGB1變化、內毒素移位情況及循環細胞因子.結果 I/R組和I/R+引流組大鼠的腸道損傷程度、內毒素水平、HMGB1和各炎癥因子水平均顯著高于空白組和假手術組(P<0.05);I/R組內毒素水平和各炎癥因子顯著高于I/R+引流組(P<0.05).免疫組織化學染色結果 顯示,I/R組的HMGBI錶達顯著高于I/R+引流組.結論 缺血再灌註損傷可導緻大鼠體內HMGB1水平升高和腸黏膜屏障損傷,HMGB1可能增加腸屏障損傷和繫統炎癥反應.腸淋巴引流能阻斷腸.淋巴途徑,改善腸屏障形態和功能,減少循環中炎癥因子和內毒素水平.
목적 연구대서장도결혈재관주손상시,내원성배체고천이솔족단백1(HMGB1)적변화급림파인류대장병장손상적영향.방법 32지건강웅성SPF급SD대서수궤분위공백조、가수술조、장도결혈재관주조(I/R)화장도결혈재관주+림파액인류조(I/R+인류조),매조8지.재결혈재관주손상후검측장도손상정도、HMGB1변화、내독소이위정황급순배세포인자.결과 I/R조화I/R+인류조대서적장도손상정도、내독소수평、HMGB1화각염증인자수평균현저고우공백조화가수술조(P<0.05);I/R조내독소수평화각염증인자현저고우I/R+인류조(P<0.05).면역조직화학염색결과 현시,I/R조적HMGBI표체현저고우I/R+인류조.결론 결혈재관주손상가도치대서체내HMGB1수평승고화장점막병장손상,HMGB1가능증가장병장손상화계통염증반응.장림파인류능조단장.림파도경,개선장병장형태화공능,감소순배중염증인자화내독소수평.
Objective To investigate the change of high mobility group box 1 ( HMGBI ) after intestine
ischemia reperfusion (I/R) in rats, compare the effect of drainage of intestine lymph fluid on gut barrier, and ex-
plore the possible mechanism of iachemia-reporfusion injury. Methods Thirty-two Sprague-Dawley (SD) rats (SPF grade) were randomly divided into4 groups with 8 rats in each group: blank group, sham group, intestine is-chemia-reperfusion (I/R) group, and intestine ischemia-reperfusion with drainage of intestine lymph fluid (I/R +drainage) group. Indicators of gut barrier function damage, translocation of endotoxin, and change of HMGB1 and cytokines were detected after intestine ischemia-reperfusion injury. Results The gut barrier function damage and levels of endotoxin, HMGBI, tumour necrosis factor-alpha ( TNF-α), interleukin-6 ( IL-6 ), interleukin-1 beta (IL-1β), and soluble intercellular adhesion molecule-1 (sICAM-1) were significantly lower in blank group and sham group than in I/R group and I/R + drainage group ( P < 0. 05 ). Compared with the intestine I/R + drainage group, the levels of endotoxin and cytokines were significantly higher in the intestine I/R group. The level of
HMGB1 was slightly higher than that in the intestine I/R + drainage group, but such difference was not statistically significant ( P > 0. 05 ). lmmunohistochemical staining also revealed that the expression of HMGB1 was significant-
ly higher in I/R group than in I/R + drainage group. Conclusions Intestine iachemia-reperfusion injury can lead to the injury of intestine mucosal barrier and increase HMGB1 level HMGB1 may deteriorate gut barrier function and increase the leveh of systemic cytokines. Drainage of lymph fluid can block the gut-lymph pathway and thus decrease the levels of endotoxin and cytokines in systemic circulation and attenuate intestine ischemia-reperfusion injury.